Blockade of c-Jun N-terminal kinase activation abrogates hyperglycemia-induced yolk sac vasculopathy in vitro

Hyperglycemia in vitro induces yolk sac vasculopathy. Embryonic malformation is inversely correlated with the yolk sac vasculature development, suggesting that hyperglycemia-induced yolk sac vasculopathy may be one of the causative factors in hyperglycemia-induced embryonic malformation. Blockade of JNK1/2 activation restores hyperglycemia-induced vasculopathy and reduces the malformation rates. These findings indicate that JNK1/2 activation mediates the deleterious effect of hyperglycemia on yolk sac vasculature and embryonic development.